Stimulants used to improve cognitive function can include the following: caffeine, nicotine, cocaine, Ritalin and Adderall. Not all of these stimulants work in the same manner. Caffeine for example, does not have any effect of the dopamine system unlike cocaine, and does not give the patient a pleasurable rush. Cocaine, Ritalin and Adderall (if it is crushed) does give the patient a rush. All these cognitive enhancers work by improving focus and energy and decreases the patients need of sleep, which means he/she can study for longer periods of time. These drugs also appear to enhance the retention of recently learned information and also improves working memory and cognitive control. However, the chronic effects of these drugs used as cognitive enhancers are not known, and that is where the risk in taking them becomes evident. It is also possible that the misuse of the prescription stimulants may make the patient dependent on their effect in order to function in their daily/academic life. Some of the most common adverse reactions of prescription stimulants are lack of appetite and difficulty sleeping as well as less common effects like, tachycardia, anxiety, tremor and headache. Some people may regard the use of cognitive stimulants as academic dishonesty and because of its unknown log-term effects it is not recommended to use these medications as a means of academic support. 

Alcohol, what is really its effect of my body.

Every heard, “we cannot start the party if there isn’t alcohol involved”, or “the only way to have fun is if we have a drink in our hand”? This is because of the “pleasant” effects that alcohol can have. Alcohol can make you feel relaxed, it can increase your self-confidence, it can make you forget about all your problems and it can make you talk more easily to other people. These effects, however, only last for a short while and then the unpleasant effects kick in, like, a decrease in judgement that can lead to doing reckless things, nausea and vomiting and blackouts. Not even to talk about the unpleasantness of a hangover you will experience the next day: a headache, sleepiness, a decrease in concentration and muscle and stomach aches. Then, how do we know how much alcohol is safe for us to drink? We use the 1-2-3-rule: 1 drink a day, no more than 2 drinks at once and do not drink more than 3 times a week.  To know when you have an alcohol drinking problem, look at your performance in school. No, not the marks that you get, but at your attention span when talking to friends, your memory of remembering stories that was told to you and your overall productivity during the day, like playing sports or any other activity that you are interested in. If you cannot concentrate or remember things or you don’t feel like playing sports or participate in any other activity that you enjoy and you know you are drinking alcohol regularly, then you must seek help, for you may have an alcohol addiction.  The best place to seek help will be to go to the school counselor, the pastor at church, or any other grown-up that you trust so that they can help you in overcoming your struggle so that you can have the bright future you deserve.

1. There are two categories of hallucinogenic drugs: classic hallucinogens and dissociative drugs.
2. Short-term effects of hallucinogenic drugs include: dizziness and sleeplessness, impulsiveness and rapid emotional shifts, euphoria, increased blood pressure, heart rate and body temperature, loss of appetite, dry mouth and sweating, numbness, weakness and tremors. The clinical profile of a patient that used hallucinogenics always include altered mental status and agitation.
3. A benzodiazepine (phenobarbital and diazepam) is given to a patient that overdosed on LSD to calm them, to reduce agitation and to normalize the operation of the CNS. For convulsions anti-epileptics can be administered. Chlorpromazine can be given to eliminate the hallucinogen and to bring back the consciousness of the patient. For vomiting, and antiemetic such as metoclopramide can be given.
4. Physostigmine, an AChE-inhibitor is given to reverse the toxicity. A benzodiazepine can also be given.

Pain:

Pain is used to describe uncomfortable sensations in the body that stems from activation of the nervous system. Pain has a broad range: it can range from annoying to debilitating, it may be consistent, it may start and stop frequently, it may only occur under certain conditions, it can develop suddenly and only last for a short period of time or it may be ongoing sensations that last or return over several months or even years.  Pain can also be described in many different ways: it may feel like a sharp stab or dull ache, it may be described as throbbing, pinching, stinging or even burning.  Pain may also be localized, only affecting a specific part of the body or it my by generalized like with overall body ached.

People also respond differently to pain: some have a high tolerance for pain and don not feel pain that easily/frequently and others have a low tolerance for pain and feel pain very intensely. Thus, pain is highly subjective.

The causes of pain can be due to a specific injury or medical condition or in some cases the cause of pain can even be less obvious or unknown. Illnesses and disorders that cause pain include: flu, arthritis, endometriosis and fibromyalgia. Pain can also be caused by bruises, burns, broken bones, etc.

Important principles of pain management include providing treatment that reduces the pain with minimal side effects, while still being able to maintain daily functions as well as preventing acute pain from progressing to chronic pain.

Medical attention is needed when the pain is a result of an injury or accident that may have caused damage to the body like bleeding, broken bones or a head injury. It is also needed when an acute, sharp internal pain is felt for it may be a sign of a serious problem like a ruptured appendix. Medical attention for pain is also needed when the pain is located in the chest, back, shoulders, neck or jaw together with other signs of a heart attack like shortness of breath, nausea, dizziness and weakness OR when the pain is interfering with your daily life, including the ability to sleep, work or taking part in any other activities that is enjoyed.

1. Mechanism of action of lithium: Lithium influences the IP3 and DAG second messenger systems by decreasing the various enzymes which are very important for conversion and re-circulation of membrane phosphoinositides.
2. The therapeutic index of lithium is 0,5-1.5mM which is very small and thus the dosing of lithium should be done very carefully and blood levels must be monitored very closely to prevent lithium toxicity.
3. Lithium as monotherapy is used for prophylaxis of manic and hypomanic episodes and treatment of an acute manic episodes. Lithium is used in combination with antidepressant for the treatment of resistant or recurrent unipolar depression and aggressive or self-mutilating behavior.
4. The renal clearance may be decreased (the toxicity be increased) by thiazide diuretics, new NSAIDs, ACE-inhibitors and fluoxetine. Renal clearance of lithium is increased by theophylline and caffeine. Lithium is neurotoxic in combination with carbamazepine, calcium-blockers, losartan, methyldopa, metronidazole and phenytoin.
5. Tremors, sedation, ataxia, aphasia, muscle weakness, fatigue, polydipsia, polyuria, nocturia, nephrogenic diabetes insipidus, thyroid enlargement, leukocytosis, edema, weight gain, acne, alopecia and sexual dysfunction.
6.  Lithium has been associated with an increased incidence of congenital cardiovascular abnormalities but the incidence is very low and when the risk-benefit has been considered it may be continued. Lithium is excreted into the breastmilk in high concentrations and thus breastfeeding is not recommended.
7.  Lithium as monotherapy is used for prophylaxis of manic and hypomanic episodes and treatment of an acute manic episodes.
8. The NSAID is causing decreased clearance of the lithium and that is why it causes an increase in the patient’s weight and other side effects of lithium are starting to arise. I would rather recommend that the patient uses Tylenol (acetaminophen) for the pain of her muscle injury for it does not have any interaction with the lithium.

1. The three phenothiazine sub-families are: Aliphatic derivatives, Piperidine derivatives and Piperazine derivatives. The aliphatic and piperidine derivatives have low potency and cause severe sedation, anti-cholinergic effects, postural hypotension and they are cardiotoxic. The Piperazine derivatives have a high potency, but it causes weaker anticholinergic effects and less sedation, less cardiovascular effects and does not cause postural hypotension.
2. Antipsychotics block D2- receptors as well as H1-receptors, cholinergic receptors and alpha1-receptors (to a lesser extent).
3. Atypical drugs block serotonin 2A-receptors whereas typical drugs block mesolimbic D2-receptors.
4. Typical drugs block D3-receptors and this causes the risk of extrapyramidal effects to reduce.
5. The phenothiazines, particularly the piperazine derivatives, have a high incidence of causing extrapyramidal side effects.
6. The blockage of cholinergic neurons by the aliphatic derivatives cause the autonomic side effects.

1. Dopamine agonists and MOA-B inhibitors.
2. Amantadine is a NMDA-antagonist that has anti-dyskinetic effects.
3. MOA-B inhibitors inhibit the MOA-B enzyme that metabolizes dopamine that then increases the dopamine stores in neurons and inhibits the uptake of dopamine in the neurons.
4. Ergot derivative: bromocriptine. Non-ergot derivatives: ropinirole, pramipexole and apomorphine.
5. Pramipexole: direct agonist at D3 receptors. Ropinirole: agonist on D2 receptors. Bromocriptine: partial agonist on D2 receptors. Apomorphine: Activates D2-receptors and to a lesser extent D1-receptors.
6. Rasagiline and selegiline are neuroprotective drugs.
7. MOA-B inhibitors inhibit the MOA-B enzyme that metabolizes dopamine that then increases the dopamine stores in neurons and inhibits the uptake of dopamine in the neurons.
8. COMT-inhibitors inhibits the COMT-enzyme that converts L-dopa to 3-O-methyl dopa. 3-O-methyl dopa produces a weak therapeutic response with L-dopa because it competes with L-dopa for the active transport process. Thus, COMT-inhibitors will decrease the metabolism of L-dopa and increases its duration of action.
9. Istradefyllin is an Adenosine A2a-antagonist. The antagonist interferes with GABA releasing and modulates ACh and dopamine release and will also facilitate dopamine receptor signaling.
10. Safinamide is used to increase dopamine activity as it is a potent, but reversible, antagonist of MAO-B. It also inhibits dopamine uptake in the neurons and decreases glutamate release.   

1. Myelinated and unmyelinated fibers:
   1. Unmyelinated fibers and smaller myelinated fibers are blocked more efficiently by local anesthetics than larger myelinated fibers. Thus, unmyelinated fibers are very sensitive to the effects of local anesthetics.
   2. When A-type fibers are blocked, proprioception, touch, pressure and motor fibers are influenced. These are the last type of fibers to be blocked by local anesthetics, thus the fibers are not that sensitive to local anesthetics.
2. Local anesthetics affect the cardiovascular tissue by causing cardiac depression. It also affects the central nervous system by producing lightheadedness, visual and auditory disturbances.
3. A local anesthetic is chosen on the type of procedure that is being done, the type of tissue that the local anesthetic must be used on and also the duration of the numbing effect that is needed in that tissue.
4. CO₂ buffers the local anesthetic. This then reduces the pain of injection and a faster onset of local anesthetics is achieved. This will also raise the effective concentration of the nonionized form of the local anesthetic, for only the nonionized form can cross the plasma membrane to have an effect, and thus the onset time of the regional block will be shortened.
5. Local anesthetics used for surface anesthesia include: oxybuprocaine, benzocaine and cocaine.   

1. Effects of inhalation anesthetics:

2. The 4 major acute toxicities of inhalation anesthetics include:

• Nephrotoxicity
• Hematotoxicity
• Malignant hyperthermia 
• Hepatotoxicity

1. Anti-epileptic drugs that decrease the effectiveness of oral contraceptives include: phenobarbitone, phenytoin, carbamazepine, oxcarbazepine and topiramate. The implications of this are that the female patient can have an unwanted pregnancy, or the patient’s hormone levels will not be regulated as it should because of the contraceptive not reaching therapeutic effective levels to prevent ovulation. Anti-epileptic drugs that are safe to use with oral contraceptives are valproate, lamotrigine, gabapentin, leviteracetam, vigabatrin.  
2. Yes, oral contraceptives can decrease serum levels of anti-epileptic drugs; examples of these drugs are: lamotrigine and valproate.
3. The metabolism of anti-epileptic drugs in neonates are slower than in an adult and the metabolism of these drugs in babies and children are faster than the metabolism in an adult. The metabolism of anti-epileptic drugs in geriatrics are also slower than in an adult, for liver and renal function are not optimal as that in a healthy younger adult.
4. Blood plasma blood levels are indicated to see how the patient’s body tolerates the medicine. The blood tests help the doctor to identify the possible allergies, interactions, infections and other abnormalities that may affect the choice of appropriate anticonvulsant medication and helps to monitor the possible drug-induced side effects. The tests are also used to monitor liver and renal function to make sure that the patient’s body can effectively metabolize the drug.